Management

1. Head Injury (HI)
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2. HI :-
– A head injury is any trauma that leads to injury of the scalp, skull, or brain
– The injuries can range from a minor bump on the skull to severe brain injury
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EPIDEMIOLOGY
• Number one killer in trauma
• 25% of all trauma deaths
• 50% of all deaths from MVA
• 200,000 people in the world live with the disability caused
by these injuries
• 50% in ages b/n 15 and 35

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ANATOMY
• Anatomy of the ’’SCALP’’
Skin
Firmly bound to the 3rd layer by perpendicular
fibers
Connective tissue
Contain blood vessels of the scalp
Aponeurosis
 fibrous sheet, found over much of the vertex
Attaches occipitalis to frontalis m
It is in this layer that - the surgeon mobilizes the scalp.

5. • Loose connective tissue
– Accounts for the mobility of the scalp
– Blood tracks freely in this layer
– bilateral orbital edema following sever head injury or cranial operation
• Periosteum
– Adheres to the suture lines of the skull
– Collection of blood beneath this layer
•  Outlines the affected bone
•  Cephalohematoma (children)
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• Anatomy of the meninges (DAP)
Dura
Endosteum and true meningeal layer
Forms falx, tentorium, diaphragm
Arachnoid
Vascular membrane
Arachnoid granulations
Pia
Highly vascular
Dips into sulci and fissures
Carries cortical vessels

8. CAUSES OF HEAD INJURY
• Road traffic accident – 80%
• Falls
• Injuries at work place, during sport, or at home
• Assaults
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RTA’s are the most common cause of TBI followed
by falls and assaults

9. CLASSIFICATIONS OF HEAD INJURY
1) Based on cause
– Primary
– Secondary
3) Based on mechanism
– Blunt
– Penetrating
• 2) Based on GCS (severity)
– Mild 14-15
– Moderate 9- 13
– severe 8 and below
• 4) Morphology
– Skull
– Intracranial lesion
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10. • Skull fracture can be
 Vault
 Basilar
• Vault fracture can also be
– Closed / open
– Linear / communited
– depressed / undepressed
• Basal skull fracture can be
– Anterior
– Middle
– Posterior
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11. 4) Anatomic
A-Extracranial
1. Scalp laceration
2. Skull vault fracture
3. Basal skull fracture
B- Intracranial
• EDH
• SDH
• SAH
• IVH
• Brain contusion ,lacerations or
DAI

12. • Head Injuries could be:
- Scalp lacerations
- Skull fractures
- Brain injury
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13. Scalp laceration
• Is a common injury.
• The clinician should identify:
– Traumatic force
– Associated symptoms of head injury
– Wound age
– Likelihood of wound contamination
– Potential presence of foreign body
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14. Skull fracture
– They occur when forces striking the head exceed the mechanical
integrity of the calvarium.
– Significant skull fractures are often accompanied by moderate or
severe intracranial injury.
– The parietal bone is most frequently fractured, followed by the
temporal, occipital, and frontal bones…….PTOF
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15. • Skull fractures themselves may or may not indicate the presence of
significant TBI.
• Certain skull fracture types, such as
– Depressed skull fractures
– Basilar skull fractures with associated cerebral spinal fluid (CSF) leak
and
– Fractures of the temporal-parietal bone that traverse the middle
meningeal artery and vein
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16. Depressed skull fracture
Indications for elevation
– Depression greater than the cranial thickness
– Intracranial hematoma
– Frontal sinus involvement
– Neurologic deficit
– Cosmetic reason
– CPD infected depressions
– Dural penetration
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17. PRIMARY INJURY TO SCALP
• Hematoma - Usually do not require Rx
- If large aspiration when it liquefies
• Wounds
Abrasions
- Cleaned & exposed
- Dressed - if hemorrhagic or serous exudate
Lacerations
- Cleaned & sutured( LA or GA)
- LA infiltrated into scalp
- Wound closure without tension
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18. PRIMARY INJURY TO SKULL
Can be vault or basal
Vault can be linear, depressed or communitted
Linear fractures
- Do not require Rx
- At temporal area  tear MMAEDH
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19. Depressed #s - simple vs open
Surgery indicated in: 3 cs
oCompression (large plate of bone)
oCosmetic area
o Compound/open wound:
 Wound debridement
 Elevate the depression
 Suture dural laceration

20. Basal skull fracture
- Fractures resulting due to blow to the occiput or
sides of the head
 Diagnosis
o History - nasal bleeding,…
o Physical examination
Raccoon eyes
Battle sign
Rhinorrhoea
Pupil size and response
Asymmetrical sluggish response
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21. • Management:
–Conservative, advise on danger sn
–Closure of dura - persistent CSF leak

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23. – If the fluid is blood tinged, the "halo" sign (also called the "ring"
or "target" sign) may be useful to determine the presence of CSF.
– To perform the test, a drop of the fluid is placed on a tissue or filter
paper.
– A rapidly expanding ring of clear fluid around red blood defines a
positive test.
– Of note, the halo test does NOT differentiate among CSF, saline,
saliva, and other clear fluids and has not been formally studied in a
clinical setting.
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24. – CSF can be distinguished from local nasal secretions more
accurately by the presence of beta-trace protein, which is found in
high concentrations in CSF or beta-2 transferrin, which is found
only in CSF, perilymph, and aqueous humor .
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25. PRIMARY BRAIN INJURY
• The damage caused to the brain at the moment of impact
Concussion
Temporary neuronal dysfunction after blunt head trauma
 Head CT is normal, &
 deficits resolve over minutes to hours
Contusion/laceration
Bruise of the brain
Breakdown of small vessels and extravasation
of blood into the brain
The frontal, occipital, and temporal poles are most often involved.
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26. Diffuse axonal injury
– Damage to axons throughout the brain
– Most frequent finding in patients who die from severe head injury
– Seen in 50% of patients who develop coma after trauma
– Due to rotational acceleration -deceleration.
– Axons may be completely disrupted and then retract.
– Small haemorrhage's can be seen in more severe cases, especially on
MRI.
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27. Mechanisms
 Coup & counter-coup injuries
 Common sites:-
– Undersurface of frontal lobe
– Tip of temporal lobe
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28. Treatment
–Cerebral contusions rarely require immediate surgical
treatment.
–Pts. must be admitted for observation as these lesions will
tend to mature and expand for 48–72 hours following injury.
–A small proportion of cerebral contusions will require
delayed surgical evacuation to reduce the mass effect.
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29. SECONDARY BRAIN INJURY
• Extra cranial
– Hypoxia
– Hypotension
– Fever
• Intracranial
– Hematoma
– Brain edema
– Raised ICP
– Infection
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30. DIAGNOSIS
History
– Age
– Loss of consciousness
– Cause, circumstance and mechanism of injury
– Presence of headache & vomiting
– Seizures
– Anticoagulant use,….
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31. ASSESSMENT OF NEUROLOGICAL FUNCTION
AND OF CONCIOUS LEVEL
• Glasgow Coma Score
• Best Eye Response (4)
– No eye opening……………………………1
– Eye opening to pain..…………………….2
– Eye opening to verbal command.……...3
– Eyes open spontaneously…...………….4
• Best Verbal Response (5)
– No verbal response ………………………1
– Incomprehensible sounds. ……………..2
– Inappropriate words. …………………….3
– Confused …………………………………..4
– Orientated …………………………………5
• Best Motor Response (6)
– No motor response.…………………..…..1
– Extension to pain.…………………….…..2
– Flexion to pain.……………………….…...3
– Withdrawal from pain..……………….…..4
– Localizing pain.……….…………….……..5
– Obeys Commands..……………………….6
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32. Exclude other causes of depressed conscious level (causes of
coma)
• No focal signs
– Drugs (alcohol, opiate)
– Circulatory collapse
– Hypothermia
– Hyperthermia
– Concussion
– Meningitis,
– Encephalitis
– Subarachnoid hemorrhage
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33. • Focal signs present
– Cerebral abscess ,
– Infarction,
– Tumor
– Intracranial hemorrhage

34. • Investigations
– Skull X-ray
– CXR and X-ray of cervical spines
– CT-Scan - first line investigation
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36. NICE guidelines for CT
– GCS < 13 at any point
– GCS 13 or 14 at 2 hours
– Focal neurological deficit
– Suspected open or depressed fracture
– Basal skull fracture
– Post-traumatic Seizure
– Persistent Vomiting > 2 episode
– Persistent headache
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37. – Coagulopathy
– Post-traumatic amnesia of >30 minutes
– Significant mechanism of injury
– Severe maxillofacial or spine injury
Urgent CT head scan if none of the above but:
• Age > 65
• Coagulopathy (e.g. on warfarin)
• Dangerous mechanism of injury (CT within 8 hours)
• Antegrade amnesia > 30 min (CT within 8 hours)

38. GENERAL MANAGEMENT OF HEAD INJURY
• ABC rule
Stabilization of airway, breathing and circulation
IV access - maintain normovolemia
- Hypotonic/glucose containing fluids should not be used b/c
hypermetabolic state
• Head end elevation - 300
• Treat co-existing injuries
Chest drain - tension pneumothorax
Cervical collar - # of cervical spine,….
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39. Indications for intubation
– GCS score of ≤8
– Motor score of ≤4
– Loss of protective laryngeal reflexes
– Ventilatory insufficiency
– Hypoxemia(pao2<60mmHg)
– Hypercarbia (arterial co2 tension i.e. paco2>45mmHg)
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40. – Spontaneous hyperventilation causing paco2 <26mmHg
– Respiratory arrhythmia
– Bilateral mandibular fracture
– Copious bleeding in to the mouth
– Seizures

41. Anticonvulsants
• May decrease early post-trauma seizures but no benefit in long term
epilepsy prevention
• Phenytoin
 Loading dose = 18 - 20 mg/kg
 Maintenance dose = 100 mg TID
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42. Patient approach
• ATLS Protocol
• Primary survey with simultaneous resuscitation
–Identify and treat what is killing the patient.
• Secondary survey
–Proceed to identify all other injuries.
• Definitive care
–Develop a definitive management plan.
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43. Taking a history in head injury
–Mechanism of injury
–Loss of consciousness or amnesia
–Level of consciousness at scene and on transfer
–Evidence of seizure
–Pre-existing medical conditions
–Medications (especially anticoagulants)
–Illicit drugs and alcohol
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44. Examination in head injury
• The general examination
• Vital signs: a combination of
– Hypertension
– Bradycardia and is known as the Cushing reflex
– Irregular respirations
• Pyrexia is seen in medullary lesion.
• Inspection and palpation of the head for skin
• Neck rigidity:
• Signs of spine trauma
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45. Examination in head injury...
• Glasgow Coma Score
• Pupil size and response
• Lateralising signs
• Signs of basal skull fracture
– Bilateral periorbital edaema (raccoon eyes)
– Battle’s sign (bruising over mastoid)
– CSF rhinorrhoea or otorrhoea
– Hemotympanum or bleeding from ear
• Full neurological examination: tone, power, sensation, reflexes
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46. Neuro sign chart every 30 min
Hx
Seizure
Headache
Vomiting
PE
BP, PR, RR, and Temperature
GCS
RBS
Oxygen saturation
Pupil size & reactivity
Limb movement
In put and out put
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47. • The following criteria must be met before discharge:
– GCS of 15
– No focal neurological deficit
– Accompanied by a responsible adult
– Should not be under the influence of alcohol or other drugs
– Verbal and written HI advice must be given
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48. Mild HI…
– Some pts. with mild HI are at significant risk of intracranial
hematoma and require CT SCAN.
– The National institute for health and clinical excellence(NICE) has
published some guidelines when to carry out a CT SCAN in a pt. with
mild HI.
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49. Traumatic Intracranial Hematomas
• Contribute to death and disability.
• Hematomas can expand rapidly and cause brain shifting and
subsequent herniation.
• Could be;
– Epidural hematoma
– Subdural hematoma
– Intraparanchymal
– Subarachnoid
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50. 1)Epidural hematoma
– Is a neurosurgical emergency.
– Also called Extradural haematoma
– The skull fracture is associated with tearing of a meningeal artery.
– Hematoma accumulates in the space between bone and dura.
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51. Intracranial Hematoma
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54. EPIDURAL HEMATOMA………..
• Usually from torn MMA (85-90%) and/or vein (10%)
• Other causes:
Torn dural sinuses(e.g: sagittal sinus)
Oozing from diploe bone & stripped Dura
• Uncommon but serious,1- 4% of TBI
• Highest among adolescents and young adults
• Skull fractures in 75-95%
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55. • The most common site is temporal, as the pterion is the thinnest part of
the skull & overlies the middle meningeal artery.
• It can also occur in other regions such as frontal & posterior fossa.
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EPIDURAL HEMATOMA

57. • Clinical presentation
Lucid interval (in 1/3 of cases) associated with headache vomiting,
drowsiness, confusion, aphasia, seizures and hemiparesis
• Patient initially complains of a headache but is fully alert and orientated
with no focal deficit.
Epidural hematoma due to venous bleeding neurologic decline is
slower but in arteries its rapid
Posterior fossa EDH - elevated ICP
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• Diagnostic evaluation
 CT scan: Lentiform ( biconvex) hyper dense
lesion
• With or without midline shift.
• Areas of mixed density may be seen in a lesion that
is actively bleeding.
• Does not cross sutural margins, but does cross
dural attachments.

59. Treatment
• Immediate surgical evacuation.
• Craniotomy / ?burr hole
Evacuation
• Prognosis-mortality -10%
• Indications for evacuation (craniotomy)
– Larger than 30 mL in volume regardless of GCS score;
– Maximum thickness >=10 mm.
– Mid-line shift >=5 mm
– EDH and coma (GCS score ≤8) who have pupillary abnormalities
(anisocoria)
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60. 2) SUBDURAL HEMATOMA
 Accumulates in the space between the dura and the arachnoid.
 Pathophysiology
Result from the tearing of bridging veins crossing the subdural space
or hemorrhage from severe cerebral contusions
 Spread more diffusely over the hemisphere than extradural and are often
associated with diffuse swelling of the underlying hemisphere
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62. Clinical manifestations - depends on type
– ASDH is nearly always associated with a significant primary brain
injury.
– Patients usually present with an impaired conscious level from the
time of injury, but further deterioration can occur.
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63. ACUTE SUBDURAL HEMATOMA
• 1-2 days after onset
Coma in (56%)
Lucid interval (12-38%)
Posterior fossa SDH - signs of increased ICP
• Result from:
Torn bridging veins
Cortical lacerations
Torn dural sinuses (common) ?
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• CT SCAN FEATURES
clot is bright or mixed-density
crescent-shaped (lunate)
may have a less distinct border
Can cross sutural margins, but is limited by dural attachments
does not cross the midline due to the presence of falx ( dural
attachement)
Is hyperdense (acute blood)
Gives diffuse and concave appearance
• Signs of mass effect:
ventricular compression, midline shift and reduction in the size of the
basal cisterns

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SUBACUTE SUBDURAL HEMATOMA
• After approximately 1-2 weeks the subdural collection become isodense to
grey matter
• detection may be challenging & recognized when:
 effacement of cortical sulci
 deviation of lateral ventricle
 midline shift
• Contrast enhancement will often define cortical-subdural interface

66. Treatment
• Evacuation via craniotomy.
• Small haematomas with little mass effect may be managed
conservatively in neurosurgical centres.
• The mortality rate from ASDH is much higher than for EDH
and is as high as 40%.
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67. Indications for Evacuation
• Acute SDH >10 mm in thickness or
• Associated with midline shift >5 mm
• If the GCS score is ≤8 or
• If the GCS score has decreased by ≥2
• The patient is with asymmetric or fixed and dilated pupils, and/or
• ICP measurements are consistently >20 mmHg
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CHRONIC SUBDURAL HEMATOMA
• after 2 weeks usually post trivial injury
due to injury of small bridging veins
headache, cognitive impairment, apathy, seizures and focal deficits
symptoms are transient and fluctuating
proximal, painless and intermittent paraparesis

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CT features
After 2 weeks, hypodense crescentic collections
Acute-on-chronic SDHs can further complicate the
images, with hyperdense fresh haemorrhage
intermixed, or layering posteriorly, within the chronic
collection
Do not cross the midline

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Management
• Acute SDH - Surgery for symptomatic & unstable pt
 Surgery
burr hole
craniotomy
 Nonoperative Mx
clinically stable
clot thickness <10mm
no clinical or CT signs of herniation
repeat CT scans 6-8 hrs after initial scan

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Chronic SDH
Surgery - burr hole
signs of increased ICP
clot thickness >10mm
cognitive impairment
motor impairment

72. Chronic subdural haematoma
• Usually occur in the elderly, alcholics and are more common in
those on anti-coagulant or anti platelet agents.
• There is usually but not always a history of minor head injury in the
weeks or months prior to presentation.
• It is thought that small bridging veins tear and cause a small ASDH
which is clinically silent.
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73. • As the haematoma breaks down it increases in volume, leading
to a mass effect on the underlying brain.
• Patients present with headache, cognitive decline, focal
neurological deficits and seizures.
• It is important to exclude hypoxic, metabolic and endocrine
disorders in this group of patients.
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74. CT appearance of CSDH
• Acute hematoma (0–10 days) is hyper-dense.
• Subacute hematoma (10 days to 2 weeks) is
iso-dense.
• Chronic hematoma (> 2 weeks) is hypo-dense.
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75. • Treatment of a CSDH and most acute-on-chronic subdural
haematomas is evacuation via burr hole.
• This is an important distinction as burr holes can be easily
performed under local anesthetic in an elderly patient with
extensive co-morbidity.
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76. RAISED INTRACRANIAL PRESSURE
• The three normal contents of the cranial vault are
–brain tissue (80%),
–blood (10%)
–CSF (10%)
• Normal state - ICP normal
4-14 mmHg - normal
>20mmHg – abnormal

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• The Monro-Kellie doctrine states that ’’the cranial vault is a rigid structure, and
therefore, the total volume of the contents determines ICP ’’
• Cerebral Perfusion Pressure (CPP) can be determined by the following formula:
CPP = MAP – ICP

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Symptoms & Signs of increased ICP
• Diminishing level of consciousness
• Headache, vomiting, seizures
• Cushing’s Triad:
• Pupillary changes
• Papilledema – most sensitive

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Effects of raised ICP
brain herniation
1) subfalcine herniation
2) uncal herniation
3) central transtentorial herniation
4) tonsillar herniation
reduced cerebral perfusion

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Management of raised ICP
• Initiated when ICP rises above 20mmHg.
• includes airway protection and adequate ventilation (intubation may be
required)
• a bolus of Mannitol 0.25-1g/kg causes:
free water diuresis
increased serum osmolality and extraction of water from the brain
• require rapid neurosurgical evaluation
• ventriculostomy or craniotomy may be needed for definitive decompression

81. MX of ICP…
In refractory cases;
Barbiturate coma
Induced hypothermia and
Decompressive caniectomy.
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83. Osmotic therapy
• By osmolar gradient, it decreases interstitial volume and then ICP.
• Mannitol;
Used most consistently to achieve ICP control.
It has also been shown to improve CBF.
It is given in boluses of 0.25 to 1 g/kg every 4 to 6 hrs as needed.
Monitoring of serum osmolality, fluid balance, renal function, and
electrolytes is required.
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84. Hyperventilation
• Control of ventilation helps prevent increases in intrathoracic
pressures that may elevate CVPs and impair cerebral venous
drainage.
• Hyperventilation decreases paco2 thereby leading to cerebral
vasoconstriction,which then results in decreased cerebral
blood volume and ICP.
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85. Hyperventilation…
• However,hyperventilation induced vasoconstriction may also cause
secondary ischemia can also increase extracellular lactate and
glutamate levels that may contribute to secondary brain injury.
• So that, it is recommended to avoid hyperventilation, especially in
the acute phase(the first 24 to 48 hrs) following TBI.
• Mild to moderate hyperventilation can be considered at later
stages, but paco2 of <30mmHg should be avoided.
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86. Sedation
• Sedation lowers elevated ICP by reducing metabolic demand.
• It may also ameliorate ventilator asynchrony and blunt
sympathetic responses of hypertension and tachycardia.
• Pentobarbital remains a RX option for elevated ICP refractory
to other therapies.
• A loading dose of 5 to 20 mg/kg is given as a bolus, followed
by 1 to 4 mg/kg per hr.
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87. Sedation…
• These drugs cause hypotension and cerebral vasodilation.
• Monitor CPP to evaluate unpredictable effects of these agents
on BP and ICP.
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88. Antiepileptic drugs
• Over all,the incidence of early post taumatic seizure is 6 to 10
% but may be as high as 30% in pts with severe TBI.
• About 15 to 25% of pts with coma and severe HI will have
nonconvulsive seizures identified on EEG.
• It has been shown to reduce the incidence of early seizures,
but does not prevent the later development of epilepsy.
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89. Reasons to prevent early seizures include
The risk of status epilepticus, which has a high fatality rate.
The potentials to aggravate systemic injury
Recurrent seizures may increase CBF could there by increase
ICP
Seizures increase a metabolic demand on damaged brain
tissue and aggravate secondary brain injury
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90. MX of Glucose
• Hyperglycemia is associated with worsened outcome in a
variety of neurologic conditions including severe TBI.
• Aggravation of secondary brain injury is by;
Increased tissue acidosis from anaerobic metabolism.
Free radical generation and
Increase BBB permeability.
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91. MX of Glucose…
• To avoid extremes of very high or low blood glucose levels, a
broad target range of upto 140 mgldl or possibly even 180
mg/dl may be appropriate.
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92. Glucocorticoids
• This therapy was found to harmful following head trauma .
DVT
Is difficult MX issue in TBI.
Can be reduced by the use of mechanical thromboprophylaxis or
antithrombotic therapy, but this has to be weighed against the
potential risk of hemorrhage expansion.
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93. Outcomes after HI
Outcome scores
• Glasgow outcome score(GOS)
Good recovery=5
Moderate disability=4
Severe disability=3
Persistent vegetative state =2
Dead =1
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94. Outcome scores…
• GOS 5 does not mean that there is no deficit but implies
independent functioning and the possibility of return to work.
• Pts with GOS 4 remain independent though with disabling deficit.
• Pts with GOS 3 are dependent on others for atleast some of their
care.
• GOS 2 pts are not aware of themselves or their environment.
• This state is not considered permanent until at least 1 yr after TBI.
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95. TECHNIQUES OF BURR HOLE AND CRANIOTOMY
BUR HOLE
Position;
• Shoulder roll,
• Head turned with side to be explored up, and
• Horse shoe head holder.
• The scalp is prepared as usual.
• For each burr hole – a straight incision 4-5cm long is made,
directed towards the vertex.
• These can be incorporated into a scalp flap if this prove necessary
for craniotomy.
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96. Standard burr hole sites
• Frontal -8cm above the superciliary ridge & 3cm
from the midline
• Parietal -on the parietal eminence
• Temporal -1cm in front of the external auditory
meatus, just above the zygomatic arch.
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97. Craniotomy
• First outline the trauma flap with a skin marker.
1. Start at the zygomatic arch <1cm anterior to the tragus.
2. Proceed superiorly and the curve posteriorly at the level of top of
the pinna.
3. 4 to 6 cm behind the pinna it is taken superiorly.
4. 1 to 2 cm ipsilateral to the midline(sagittal suture) curve ateriorly
to end behind the hairline.
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98. 12/28/2023 gkg 98
COMPLICATIONS HEAD INJURY
• Meningitis & brain abscess
• CSF rhinorrhea and otorrhea
• Epilepsy - about 80% arise in 2yrs
• Hydrocephalus- usually due to atrophied white matter
• Amnesia (PTA)
• Postconcussional Sx
• Posttraumatic encephalopathy
• Cranial nerve injury - in up to 30% pts

99. SUMMARY
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100. Investigations
• CBC
• RBS
• RFT
• LFT
• Electrolytes
• ABG analysis
• ECG
• CXR-aspirations
• Skull X-Ray-vault fractures

101. Management
General
• ABC with C –spine protection
• IV line and isotonic fluids
• Catheterization
• NGT feeding
• 100% Oxygen
• GI prophylaxis
• DVT prophylaxis
• Anti pain & antipyretics
• Neuro sign & glucose monitoring
ICP MX
• Head elevation to 30 degree
• Hyperventilation
• Osmotic diuresis
• Hypertonic saline
• Then specific mx

102. 102

103. Skull fracture
• Linear fractures are the most
common, followed by depressed
and basilar skull fractures.

104. 104

105. 105

106. 106